Mads Tang-Christensen: The brain science of obesity | TED

Transcriber:

譯者: Camila Lin 審譯者: Helen Chang

Have you ever wondered why a pair of siblings

你們有沒有想過， 為什麼一對兄弟姊妹，

living in the same house with the same parents,

住在同樣的屋子裡，有相同的父母，

with the same food,

吃一樣的食物，

sometimes end up in opposite sides of the weight spectrum?

他們的體重有時候卻完全相反？

My name is Mads

我叫麥斯，

and for the last 25 years,

這25年來，

I've been studying what we eat, when we eat and how much we eat.

我都在研究我們吃什麼、 什麼時候吃、吃了多少。

And probably more importantly,

更重要的是，

I've been studying how each of our unique bodies

我一直在研究每個人獨特的身體，

responds differently to the same food and the same environment.

為何會對同樣的食物和環境 產生不同反應。

To be more precise, I study obesity.

說得更清楚一點，我研究肥胖。

During my training as an MD, PhD,

在我攻讀醫學博士時，

I was very fascinated by a series of experiments done by Barry Levin.

我非常著迷於貝瑞‧萊文 做的一系列實驗。

He took 100 rats and subjected them to high-fat feeding.

他選了一百隻老鼠， 並強迫牠們吃高脂肪的食物。

After months of feeding,

在數個月的餵食後，

he ended up with a bell-shaped curve

他最後畫出一個 紀錄老鼠體重的鐘形曲線：

and a weight distribution

with some skinny rats and some obese rats

有些老鼠很瘦，有些老鼠很胖，

and some in the middle.

有些老鼠的體重則在中間。

What he then did was to take the skinny rats

之後，他單獨取出瘦的老鼠，

and breed them among themselves,

讓牠們繁衍下一代，

and the heavy rats.

也特別取出那些胖的老鼠，

And he bred those among themselves.

讓牠們繁殖下一代。

And after rounds of breeding, he ended up with two distinct populations:

在數輪的繁衍之後， 他有了兩群體質完全不同的老鼠：

a diet-resistant rat

耐瘦的老鼠，

and an obesity-prone rat.

和易胖的老鼠。

And here's the really interesting part.

而這是整個實驗最有趣的地方：

Then he took the skinny or the obese,

他取出瘦的老鼠或胖的老鼠，

and either massively over- or underfed them.

要嘛大量餵食，要嘛完全不餵牠們。

And their weight would, of course, go up and down

而牠們的體重，

depending on the dietary regimen.

就隨著當時的餵食方案起起落落。

But it was as if the little bodies would remember the same old weight trajectory.

但牠們的小身體就好像 記得以前的體重軌跡一樣，

So once the dietary regimen was stopped,

所以一旦暫停餵食方案，

the rats went right back to the initial weight trajectory.

這些老鼠的體重就會回到原狀。

It was like as if you could dress up the obese rat

就好像你雖然能將胖老鼠塞到

in a skinny sheep's clothing.

瘦羊的皮囊裡面，

But the obese rat nature was still scratching to get out.

但胖老鼠的天性還是 想方設法地跑出來。

The same thing applies to humans.

人也是如此。

If you take a thousand kids and weigh them,

如果你選出一千個小孩， 為他們量體重，

their weight will also be distributed in a bell-shaped curve.

他們的體重分布也會呈現鐘形曲線。

Some skinny, some in the middle and some heavy.

有些很瘦，有些在中間，有些則過重。

We know that some of the skinny kids will remain skinny throughout life,

我們知道，有些瘦小孩 一輩子都會這麼瘦，

and some of the obese kids will stay obese throughout life.

有些胖小孩則會一生都很胖。

You could argue that their weight, to some degree, has been predetermined.

你可以說，以某種程度而言， 他們的體重已經天生註定了。

You could also argue that obesity is a disease.

你也可以說，肥胖是一種病。

Wait, did I just say that obesity a disease?

等等，我剛剛是說肥胖是一種病嗎？

Yes.

沒錯。

There's actually data and science that shows that.

實際上，已經有科學數據能證明這點。

And I've made it my audacious life goal to come up with a solution

我也把找出預防、對待， 甚至治癒肥胖的解答，

to prevent, treat or even cure obesity.

做為我大膽的生涯目標。

Let me explain.

讓我解釋。

In the early 1980s and 1990s,

在 1980 和 1990 年代早期，

obesity was considered a potential global problem,

肥胖被視為潛在的全球問題，

a global problem of a magnitude

而且是嚴重的全球問題。

that led WHO in the end of 1990s

因此，世界衛生組織 在 1990 年代末期

to declare obesity a global pandemic.

宣布肥胖已成為全球性的流行病。

And I probably don't have to tell you why.

我應該不用多說什麼。

Higher rates of diabetes, hypertension, cardiovascular disease, even some cancers,

更易罹患糖尿病、高血壓、心血管 疾病，甚至是某些癌症及骨關節炎，

osteoarthritis and a clear link to mental conditions such as depression.

同時也和特定心理狀態 如憂鬱症明顯相關。

So as the number of obese individuals grew,

所以隨著肥胖成人越來越多，

so did the number of people suffering from these diseases.

受這些疾病所苦的人也越來越多。

Today, more than 50 percent of the US adult population

現在，有超過一半的美國成人，

are living with obesity or overweight.

處於過重或肥胖的狀態中。

From a health perspective, that is devastating.

從健康的角度來看， 這是非常可怕的大問題。

But it's not only a US problem.

但這不只是美國的問題。

The obesity surge has made obesity a global health problem.

急遽增加的肥胖人數， 已讓肥胖成為全球性的健康問題。

Many inside and outside the medical community

不論醫學界內外，

believe obesity is not a disease.

許多人都相信肥胖不是一種病。

They believe that obesity is a condition,

他們認為肥胖是一個狀態，

a condition brought about by too much eating

會達到這個狀態

是因為過度飲食和過少的運動量。

and too little exercise.

As a matter of fact, a lot of people living with obesity think that too.

實際上，許多肥胖的人也這樣想。

They believe that their weight is 100 percent their own fault,

他們相信，他們的體重 百分百都是自作孽，

which can lead to self-blame and low self-esteem,

而這個認知會導致自責和低自尊，

and perhaps even shame or stress eating,

甚至帶來羞恥或壓力性進食，

which is both heartbreaking, as well as counterproductive.

這個結果讓人心碎，也完全是反作用。

But where is the scientific proof that obesity is a disease?

但證明肥胖是病的科學證據在哪？

Well, medically speaking, there's many ways to define disease,

從醫學的角度來說， 有很多方法能定義疾病，

but let me give you just three examples.

但讓我給你們三個例子。

As a process that impairs your functionality

「一種損壞身體機能， 並降低生活期望的過程。」

and reduces life expectancy -- obesity, check.

肥胖符合這個條件。

You can define disease as a process

你可以將疾病定義為

「更易受其他疾病影響 或導致疾病的一種過程」，

that leaves you more susceptible to other diseases or causes disease.

Obesity, check.

肥胖符合這個條件。

Or you can define disease as a genetic impairment

或者你也可以將疾病定義為

「基因缺陷所導致的身體機能缺陷」，

that leads to functional impairment,

like, for instance, a duplication of genes on chromosomes.

例如染色體上重複的基因。

There is clear evidence

有明顯的證據證明，

that a single gene mutation can lead to obesity,

有一個突變基因會導致肥胖，

such as, for instance, leptin deficiency and POMC deficiency.

例如缺乏瘦體素 或是前腦啡黑細胞促素皮促素。

We also have two-three genes leading to obesity.

我們也有數個能導致肥胖的基因。

And it's my prediction that we, by the year 2030,

我預測在 2030 年，

will be able to explain most obesity by the genetic makeup of the individual.

我們就能用個體的基因序列 解釋大多數的肥胖。

So obesity as a disease by this measure, check.

因此以這個標準而言，肥胖是疾病。

Let me be clear.

讓我說清楚。

We humans have had the same genes for decades.

我們人類數十年來的基因都相同。

And just recently, obesity has become a bigger problem.

但直到最近，肥胖才變成 一個比較嚴重的問題。

How do we then explain that?

這又該怎麼解釋？

One obvious thing is actually food, especially calorie-rich food,

最明顯的一件事就是食物， 特別是滿滿卡路里的食物，

which is much more readily available.

也是更容易取得的食物。

It's relatively easy and also relatively cheap

相較而言，這種食物更方便也更便宜，

to eat your entire daily need of calories by a fast food or big soft drinks.

一份速食或一大杯軟性飲料， 就能滿足你一天需要的熱量。

So genes do play a role,

所以基因雖然也是原因之一，

but the environment also plays a huge role.

但環境造成的影響更大。

The overabundance of calories in certain communities

特定社群攝取的過度熱量，

is a relatively new thing,

是近幾年才發生的事，

and our genes haven't quite adapted yet.

因此我們的基因還沒 完全適應這個轉變。

In the history of feast and famine,

在盛宴和飢荒的歷史中，

genetic selection has prepared us much better for famine,

基因選擇讓我們更能適應飢荒，

and for good reason.

這有個好理由：

Starvation is bad,

飢餓很糟糕。

but you could also argue obesity is bad.

但你也能說肥胖很糟糕。

And if obesity is a disease,

那如果肥胖是一種疾病，

how do we then prevent, treat or even cure it?

我們要怎麼預防、應對甚至治療它？

I believe that the brain holds the key.

我相信解決辦法就在大腦。

I have always been fascinated

我一直都對大腦不同部位的微小電訊號

with how small electrical signals in discrete parts of the brain

是如何導致巨大的行為改變很有興趣。

lead to big behavioral changes.

是如何導致巨大的行為改變很有興趣。

And my study of the brain led me to Glucagon-Like Peptide 1,

我對大腦的研究，讓我注意到 「昇糖素類似胜肽」，

or GLP-1 for short.

它的簡稱是 GLP-1 。

GLP-1 is a hormone and a signal molecule

這是一種消化道和大腦都會分泌的

that is produced both in the gut and in the brain.

荷爾蒙和傳訊分子。

The brain speaks to the gut and the gut speaks to the brain.

大腦和腹部彼此傳遞訊息給對方。

Yes, that's right.

沒錯，這是正確的。

Your belly and your brain are literally connected.

你的肚子真的和你的大腦連在一起。

Our research led us to see that GLP-1 has an effect on nerve cells

我們的研究讓我們發現，

GLP-1 能對決定我們是否 進食的神經細胞產生影響，

sitting in areas that control whether we eat or not.

So, for instance, if we increase the level of GLP-1,

所以，舉例來說， 如果我們提高它的濃度，

the body's desire to eat or overeat food gets turned off.

就能澆熄身體想要進食或暴食的慾望。

GLP-1 serves as the full signal in your car's gas tank.

GLP-1 的功用就像是 車子油箱中的滿溢訊號。

I've spent years and decades mapping the circuitry of GLP-1

我花了幾十年標記出 GLP-1 的作用循環，

and how GLP-1 interacts with other signal molecules and hormones.

以及它如何和其他傳訊分子 及賀爾蒙交互作用。

All of these things go together and control food intake,

這些東西彼此影響，控制我們的進食、

body weight and the control of eating behavior.

體重及飲食習慣。

And what does that all mean?

這是甚麼意思？

Well, today, we have engineered and studied the molecule,

現在，我們已經研究並造出這個分子，

so we now have a molecule

所以我們現在有了一種

that can lead to a significant weight loss.

能讓體重顯著降低的分子。

Obviously, GLP-1 is not the whole answer.

很顯然 GLP-1 不是全部的答案。

We and others have discovered numerous hormones

我們和其他人發現了數種

and other signal molecules

也在規律攝取食物及體重上 扮演關鍵角色的

that are also pivotal for the regulation of food intake and body weight.

荷爾蒙和其他傳訊分子。

And it may end up

也很有可能，

that these signal molecules and hormones are even more important than GLP-1.

這些傳訊分子與賀爾蒙 最後比 GLP-1 更重要。

So ...

所以，

There's plenty for us to do.

還有很多事情等著我們去做。

There's still plenty for us to explore.

還有很多東西等著我們去探索。

So this is not the end.

所以這不是結束，

It's not even the beginning to the end.

甚至不是抵達終點的第一步。

But perhaps this may be the end to the beginning.

但也許這會是開始的最後一步。

We may have a massive weight crisis on the planet today,

現在我們的世界可能會 發生嚴重的肥胖問題。

but the good news is we are on the right path.

但好消息是，我們走在正確的路上。

We now have solutions for people living with obesity,

我們現在已經有了給肥胖人士的解方，

and the next steps will be to understand even better

下一步就是更了解

the problems people living with obesity are facing.

肥胖者面臨的那些問題。

To understand even better how genes and environment play together.

更了解基因和環境如何交互作用。

And understand, finally, how all these things come together

接著了解，這些事情如何互相影響

and determine our body weight.

最終決定我們的體重。

Then, and maybe just then,

然後，或許這樣一來，

we will be able to come up with a prevention,

我們就能夠為肥胖人士，

a treatment or even a cure

找出預防肥胖、

for people living with obesity,

應對肥胖，甚至是治療肥胖的方法，

like we strive for with any other chronic disease.

就像是我們對其他慢性病做的一樣。

And this -- this still remains our audacious life’s goal.

而這，這還是我們大膽的生涯目標。

Thank you.

謝謝。